Hormesis and exercise: How the cell copes with oxidative stress

Li Li Ji, Zsolt Radak, Sataro Goto

Research output: Contribution to journalReview articlepeer-review

18 Scopus citations


Contraction-induced production of reactive oxygen and nitrogen species has been shown to cause oxidative stress to skeletal muscle, heart and other organs. As an adaptive response, muscle antioxidant defense systems are upregulated in response to exercise to restore intracellular prooxidant-antioxidant homeostasis. Thus, both young and old animals and humans involved in regular exercise have shown reduced oxidative damage during acute physical exertion at accustomed or excessive intensity, or under oxidative challenges otherwise deemed detrimental. The current article provides a brief review of this exercise-induced hormesis with the emphasis on the role of redox sensitive signal transduction pathways (mainly nuclear factor κB and mitogen-activated protein kinase) that can activate the gene expression of antioxidant enzymes and proteins. Molecular mechanisms and gene targets for these signaling pathways, as well as the biological significance of the adaptations, are discussed.

Original languageEnglish (US)
Pages (from-to)41-55
Number of pages15
JournalAmerican Journal of Pharmacology and Toxicology
Issue number1
StatePublished - 2008


  • Antioxidant
  • Exercise
  • Oxidative stress
  • Reactive oxygen species
  • Signaling


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